scholarly journals Local Cerebral Blood Flow during Lithium–Pilocarpine Seizures in the Developing and Adult Rat: Role of Coupling between Blood Flow and Metabolism in the Genesis of Neuronal Damage

2002 ◽  
Vol 22 (2) ◽  
pp. 196-205 ◽  
Author(s):  
Anne Pereira de Vasconcelos ◽  
Arielle Ferrandon ◽  
Astrid Nehlig
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Status Epilepticus ◽  
Metabolic Rate ◽  
Neuronal Damage ◽  
Adult Brain ◽  
Local Cerebral Blood Flow ◽  
Adult Rats ◽  
Flow Rates ◽  
Cerebral Metabolic Rate

Coupling between local cerebral blood flow and local cerebral metabolic rate for glucose is involved in the pathogenesis of epilepsy-related neuronal damage in the adult brain; however, its role in the immature brain is unknown. Lithium–pilocarpine–induced status epilepticus is associated with extended damage in adult rats, mostly in the forebrain limbic areas and thalamus, whereas damage was moderate in 21-day-old rats (P21) or absent in P10 rats. The quantitative autoradiographic [14C]iodoantipyrine technique was applied to measure the consequences of lithium-pilocarpine status epilepticus on local cerebral blood flow. In adult and P21 rats, local cerebral blood flow rates increased by 50% to 400%; the highest increases were recorded in regions showing damage in adults. At P10, local cerebral blood flow rates decreased by 40% to 60% in most areas, except in some forebrain regions showing no change during status epilepticus. In areas injured when status epilepticus was induced in adults, a strong hypermetabolism ( Fernandes et al., 1999 ) not matched by comparable local cerebral blood flow increases was present in rats of all ages, whereas in damage-resistant areas, local cerebral metabolic rate for glucose and local cerebral blood flow remained coupled in the three age groups. Thus, the level of coupling between blood flow supply and metabolism is not involved in seizure-related brain damage in the developing brain, which appears to be resistant to the consequences of such a mismatch.

scholarly journals Effects of Pentylenetetrazol-Induced Status Epilepticus on Local Cerebral Blood Flow in the Developing Rat

1995 ◽  
Vol 15 (2) ◽  
pp. 270-283 ◽  
Author(s):  
Anne Pereira de Vasconcelos ◽  
Sylvette Boyet ◽  
Violette Koziel ◽  
Astrid Nehlig
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Status Epilepticus ◽  
Dentate Gyrus ◽  
Dorsal Hippocampus ◽  
Adult Brain ◽  
Local Cerebral Blood Flow ◽  
Flow Response ◽  
Age Dependent ◽  
Developing Rat

The quantitative autoradiographic [14C]-iodoantipyrine technique was applied to measure the effects of a 30-min period of pentylenetetrazol (PTZ)-induced status epilepticus (SE) on local cerebral blood flow (LCBF) in rats 10 (P10), 14 (P14), 17 (P17), and 21 (P21) days after birth. The animals received repetitive, timed injections of subconvulsive doses of PTZ until SE was reached. At P10, SE induced a 32 to 184% increase in the rates of LCBF affecting all structures studied. In P14- and P17 PTZ-treated rats, LCBF values significantly increased in two-thirds of the structures belonging to all systems studied and were not changed by SE in the parietal cortex, dorsal hippocampus, and dentate gyrus. At P21, rates of LCBF were still increased in 48 of the 73 structures studied; however, LCBF values were decreased by SE in most cortical areas, the hippocampus, and the dentate gyrus. CBF and cerebral metabolic rate for glucose (CMRglc) remained coupled in both controls and PTZ-exposed rats. Our results show that changes in LCBF with seizures are age dependent. At the most immature ages, P10 and P14, both LCBF and local CMRglc (LCMRglc) values are largely increased by long-lasting seizures. At P17 and P21, the blood flow response to SE becomes more heterogeneous, with specific decreases in the hippocampus and cortex at P21. The absence of mismatch between LCBF and LCMRglc in PTZ-exposed rats at all ages may explain at least partly why the immature brain is more resistant to seizure-induced brain damage than the adult brain.

Vasopressin and prostanoid mechanisms in control of cerebral blood flow in hypotensive newborn pigs

1990 ◽  
Vol 258 (2) ◽  
pp. H408-H413 ◽  
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Metabolic Rate ◽  
Cerebral Vasoconstriction ◽  
Newborn Pigs ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

scholarly journals Effect of stage 2 kindling on local cerebral blood flow rates in rats with genetic absence epilepsy

Epilepsia ◽  
2009 ◽  
Vol 50 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Nihan Çarçak ◽  
Arielle Ferrandon ◽  
Estelle Koning ◽  
Rezzan Gülhan Aker ◽  
Osman Özdemir ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Absence Epilepsy ◽  
Local Cerebral Blood Flow ◽  
Flow Rates

scholarly journals Acute hypoxia increases the cerebral metabolic rate – a magnetic resonance imaging study

2015 ◽  
Vol 36 (6) ◽  
pp. 1046-1058 ◽  
Author(s):  
Mark B Vestergaard ◽  
Ulrich Lindberg ◽  
Niels Jacob Aachmann-Andersen ◽  
Kristian Lisbjerg ◽  
Søren Just Christensen ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Oxygen Saturation ◽  
Healthy Subjects ◽  
Acute Hypoxia ◽  
Resonance Imaging ◽  
Cerebral Metabolic Rate

The aim of the present study was to examine changes in cerebral metabolism by magnetic resonance imaging of healthy subjects during inhalation of 10% O2 hypoxic air. Hypoxic exposure elevates cerebral perfusion, but its effect on energy metabolism has been less investigated. Magnetic resonance imaging techniques were used to measure global cerebral blood flow and the venous oxygen saturation in the sagittal sinus. Global cerebral metabolic rate of oxygen was quantified from cerebral blood flow and arteriovenous oxygen saturation difference. Concentrations of lactate, glutamate, N-acetylaspartate, creatine and phosphocreatine were measured in the visual cortex by magnetic resonance spectroscopy. Twenty-three young healthy males were scanned for 60 min during normoxia, followed by 40 min of breathing hypoxic air. Inhalation of hypoxic air resulted in an increase in cerebral blood flow of 15.5% ( p = 0.058), and an increase in cerebral metabolic rate of oxygen of 8.5% ( p = 0.035). Cerebral lactate concentration increased by 180.3% ([Formula: see text]), glutamate increased by 4.7% ([Formula: see text]) and creatine and phosphocreatine decreased by 15.2% ( p[Formula: see text]). The N-acetylaspartate concentration was unchanged ( p = 0.36). In conclusion, acute hypoxia in healthy subjects increased perfusion and metabolic rate, which could represent an increase in neuronal activity. We conclude that marked changes in brain homeostasis occur in the healthy human brain during exposure to acute hypoxia.

scholarly journals Cerebral Effects of Propofol following Bolus Administration in Sheep

1996 ◽  
Vol 24 (1) ◽  
pp. 26-31 ◽  
Author(s):  
G. L. Ludbrook ◽  
R. N. Upton ◽  
C. Grant ◽  
E. C. Gray
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Electrical Stimulus ◽  
Bolus Administration ◽  
Depth Of Anaesthesia ◽  
Cerebral Metabolic Rate ◽  
Deep Anaesthesia ◽  
Dose Dependent ◽  
Withdrawal Response

The effects of bolus administration of propofol (50 mg, 100 mg and 200 mg) on cerebral blood flow and cerebral metabolic rate for oxygen were examined in a chronically catheterized sheep preparation. Depth of anaesthesia was simultaneously measured using a withdrawal response to a noxious electrical stimulus and it was demonstrated that the 100 mg dose induced moderate sedation while the 200 mg dose induced relatively deep anaesthesia. Propofol caused transient dose-dependent decreases in cerebral blood flow, despite minimal changes in blood pressure. These were accompanied by parallel decreases in cerebral metabolic rate but no change in cerebral oxygen extraction. As cerebrovascular responses in the sheep appear similar to those in man, the parallel changes in cerebral blood flow and metabolic rate demonstrated in this study supports the suitability of propofol as a neuroanaesthetic agent.

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